ReviewCell death and differentiation2022
Should mutant TP53 be targeted for cancer therapy?
Review in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
100 citing papers in PubMed, 146 citations in OpenAlex.
- UBE2A as a prognostic indicator across human cancers: Insights from multi‑omics and immune landscape analyses.Molecular medicine reports · 2026Article
- Study on the carcinogenic risk of food preservatives and their related molecular targets and pathway mechanisms through network toxicology analysis.Molecular diversity · 2026Article
- Tumor heterogeneity: development, mechanisms, and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- MiR-4327 targets TP53 to promote cervical cancer cell proliferation.Functional & integrative genomics · 2026Article
- The prognostic value of different HPV infection statuses in cervical cancer.Scientific reports · 2026Observational
- Genetic mutations in primary and metastatic tumors of a rare mixed neuroendocrine carcinoma and high-grade serous ovarian cancer.Medical molecular morphology · 2026Article
- Fundamentals and emerging frontiers in p53-targeted drug development.Biochemistry and biophysics reports · 2026Review
- Comprehensive analysis of metabolic reprogramming-related gene signatures for predicting ovarian cancer prognosis, the immune landscape, and potential treatment options.Discover oncology · 2026Article
- Brain Cancer: Molecular Alterations and Emerging Trends in Neuropharmacology.International journal of molecular sciences · 2026Review
- The Enigmatic Tumor Suppressor p53 Biomolecule: Its Role and Prognostic and Predictive Values in Cancer Therapy and Precision Medicine.Biomolecules · 2026Review
- Genomic characterization of DNA damage response pathway mutations reveals their adverse impact on EGFR-TKI efficacy in non-small cell lung cancer.Respiratory research · 2026Article
- CBC3T-3: a novel patient-derived cisplatin-resistant distal cholangiocarcinoma cell line harboring multiple TP53 missense mutations.Human cell · 2026Article
- From Metabolism to Longevity: Molecular Mechanisms Underlying Metformin's Anticancer and Anti-Aging Effects.Current issues in molecular biology · 2026Review
- Pro-ATO/Allicin Liposomes for Dual-Pathway Targeting of p53-Mutant Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Prognostic Biomarkers and Immunotherapeutic Insights of Circulating Tumor DNA Analysis in Advanced Esophageal Squamous Cell Carcinoma From SCRUM-MONSTAR GOZILA Substudy.JCO precision oncology · 2026Article
- Construction and validation of a palmitoylation-related prognostic model for lung adenocarcinoma based on integrated bioinformatics and machine learning.Translational cancer research · 2026Article
- TP53 mutation predict poor prognosis in diffuse large B-cell lymphoma: a single-center study.Annals of hematology · 2026Article
- Deciphering stromal cell interactions in osteosarcoma highlights CDKN2A and MMP14 as novel diagnostic and therapeutic biomarkers.European journal of medical research · 2026Article
- Knockdown of caspase-activated DNase and B-cell lymphoma 2 inhibits cell proliferation and drug resistance in TP53-mutant multiple myeloma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- The value of DNA repair gene and TP53 co-mutation in predicting the response of non-small cell lung cancer to immunotherapy.Discover oncology · 2026Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the TP53 tumour suppressor gene are found in ~50% of human cancers [1-6]. TP53 functions as a transcription factor that directly regulates the expression of ~500 genes, some of them involved in cell cycle arrest/cell senescence, apoptotic cell death or DNA damage repair, i.e. the cellular responses that together prevent tumorigenesis [1-6]. Defects in TP53 function not only cause tumour development but also impair the response of malignant cells to anti-cancer drugs, particularly those that induce DNA damage [1-6]. Most mutations in TP53 in human cancers cause a single amino acid substitution, usually within the DNA binding domain of the TP53 protein. These mutant TP53 proteins are often expressed at high levels in the malignant cells. Three cancer causing attributes have been postulated for mutant TP53 proteins: the inability to activate target genes controlled by wt TP53 (loss-of-function, LOF) that are critical for tumour suppression, dominant negative effects (DNE), i.e. blocking the function of wt TP53 in cells during early stages of transformation when mutant and wt TP53 proteins are co-expressed, and gain-of-function (GOF) effects whereby mutant TP53 impacts diverse cellular pathways by interacting with proteins that are not normally engaged by wt TP53 [1-6]. The GOF effects of mutant TP53 were reported to be essential for the sustained proliferation and survival of malignant cells and it was therefore proposed that agents that can remove mutant TP53 protein would have substantial therapeutic impact [7-9]. In this review article we discuss evidence for and against the value of targeting mutant TP53 protein for cancer therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.